title: Regulation of miR-155 affects pancreatic cancer cell invasiveness and migration by modulating the STAT3 signaling pathway through SOCS1.
abstract: In the present study, we investigated the effects of miR-155 on pancreatic cancer cell invasion and migration in vitro, underlying gene expression, expression of miR-155 and its target genes in pancreatic cancer tissues, and their association with metastasis and clinical stage. miR-155 mimics and an inhibitor were transfected into Panc-1 and Capan-2 cells in order to regulate the expression of miR-155. qPCR and western immunoblotting were performed in order to detect gene expression. Transwell assays were performed to characterize the invasion and migration of pancreatic cancer cells in vitro. Immunohistochemical analysis and in situ hybridization were used to detect the expression of protein and microRNA in pancreatic cancer tissue. miR-155 mimics and an inhibitor upregulated and downregulated, respectively, the expression of miR-155 in pancreatic cancer cells. The invasion and migration of pancreatic cancer cells increased or decreased along with miR-155 expression in vitro. Suppressor of cytokine signaling 1 (SOCS1) protein expression was upregulated when miR-155 was inhibited and downregulated when miR-155 was increased. However, the expression of P-signal transducer and activator of transcription-3 (STAT3) was synchronized with that of miR-155. Transcription of SOCS1 and STAT3 was unchanged by miR-155 regulation. miR-155 expression was high in pancreatic cancer tissues and SOCS1 expression was high in tumor-adjacent tissues. There was no relationship between these genes in cancer and tumor-adjacent tissues. In addition, miR-155 expression was associated with lymph node metastasis and clinical stage. In conclusion, miR-155 plays an important role in the regulation of pancreatic cancer cell invasion and migration by modulating the STAT3 signaling pathway and reducing SOCS1 expression in pancreatic cancer cells.
authors.affiliation: Department of General Surgery, Affiliated First People's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200080, P.R. China.
authors.forename: Chen
authors.initials: C
authors.lastname: Huang
authors.forename: Haidong
authors.initials: H
authors.lastname: Li
authors.forename: Weidong
authors.initials: W
authors.lastname: Wu
authors.forename: Tao
authors.initials: T
authors.lastname: Jiang
authors.forename: Zhengjun
authors.initials: Z
authors.lastname: Qiu
mesh_terms: D017209:Apoptosis; D015153:Blotting, Western; D002465:Cell Movement; D049109:Cell Proliferation; D005434:Flow Cytometry; D006801:Humans; D007124:Immunoenzyme Techniques; D017403:In Situ Hybridization; D008207:Lymphatic Metastasis; D035683:MicroRNAs / Q000235:genetics*; D009361:Neoplasm Invasiveness; D009367:Neoplasm Staging; D010190:Pancreatic Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology*; D011379:Prognosis; D012333:RNA, Messenger / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D020133:Reverse Transcriptase Polymerase Chain Reaction; D050796:STAT3 Transcription Factor / Q000235:genetics / Q000378:metabolism*; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins / Q000235:genetics / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: C524942:MIRN155 microRNA, human; D035683:MicroRNAs; D012333:RNA, Messenger; C108944:SOCS1 protein, human; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D000071222:Suppressor of Cytokine Signaling 1 Protein; D050826:Suppressor of Cytokine Signaling Proteins